Changes in aortic endothelial gene expressions and relaxation responses following chronic short-term insulin treatment in diabetic rats

Kobayashi, Tsuneo; Oishi, Keiji; Hayashi, Yuko; Matsumoto, Takayuki; Kamata, Katsuo

doi:10.1016/j.atherosclerosis.2005.05.026

Cited by 14 publications

(6 citation statements)

References 38 publications

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“…However, the results of the present study are consistent with those of De Vriese and colleagues (4), who demonstrated in STZ diabetic rats treated with insulin, that the global RBF response to a 100 ng intrarenal bolus dose of ACh was attenuated compared with control animals. Evidence from in vitro studies of arteries from a number of different vascular beds indicates that insulin treatment and improved metabolic control can improve endothelium-dependent vasodilation in diabetes (12,17,31). The extent of improvement does vary with the vascular bed and how well the hyperglycemia is controlled.…”

Section: Discussionmentioning

confidence: 99%

In vivo regulation of endothelium-dependent vasodilation in the rat renal circulation and the effect of streptozotocin-induced diabetes

Edgley

Tare²,

Evans³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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Edgley AJ, Tare M, Evans RG, Skordilis C, Parkington HC. In vivo regulation of endothelium-dependent vasodilation in the rat renal circulation and the effect of streptozotocin-induced diabetes. Am J Physiol Regul Integr Comp Physiol 295: R829 -R839, 2008. First published July 16, 2008 doi:10.1152/ajpregu.00861.2007.-We assessed the relative contributions of endothelium-derived relaxing factors to renal vasodilation in vivo and determined whether these are altered in established streptozotocin-induced diabetes. In nondiabetic rats, stimulation of the endothelium by locally administered ACh or bradykinin-induced transient renal hyperemia. Neither basal renal blood flow (RBF) nor renal hyperemic responses to ACh or bradykinin were altered by blockade of prostanoid production (indomethacin) or by administration of charybdotoxin (ChTx) plus apamin to block endothelium-derived hyperpolarizing factor (EDHF). In contrast, combined blockade of nitric oxide (NO) synthase, N -nitro-L-arginine methyl ester (L-NAME), and prostanoid production reduced basal RBF and the duration of the hyperemic responses to ACh and bradykinin and revealed a delayed ischemic response to ACh. Accordingly, L-NAME and indomethacin markedly reduced integrated (area under the curve) hyperemic responses to ACh and bradykinin. Peak increases in RBF in response to ACh and bradykinin were not reduced by L-NAME and indomethacin but were reduced by subsequent blockade of EDHF. L-NAME plus indomethacin and ChTx plus apamin altered RBF responses to endothelium stimulation in a qualitatively similar fashion in diabetic and nondiabetic rats. The integrated renal hyperemic responses to ACh and bradykinin were blunted in diabetes, due to a diminished contribution of the component abolished by L-NAME plus indomethacin. We conclude that NO dominates integrated hyperemic responses to ACh and bradykinin in the rat kidney in vivo. After prior inhibition of NO synthase, EDHF mediates transient renal vasodilation in vivo. Renal endotheliumdependent vasodilation is diminished in diabetes due to impaired NO function. kidney circulation; acetylcholine; bradykinin; endothelium-derived hyperpolarizing factor; nitric oxide THE VASCULAR ENDOTHELIUM MEDIATES relaxation of the underlying smooth muscle via the actions of several vasodilators, including nitric oxide (NO), prostanoids (e.g., prostacyclin), and an endothelium-derived hyperpolarizing factor (EDHF) (36). The relative importance of these vasodilators varies across different vascular beds (32). While NO is critical in the larger vessels, EDHF assumes greater importance in smallresistance arteries (34).Endothelium-derived NO, prostanoids, and EDHF have all been implicated in the control of renal vascular tone in vitro. Inhibition of NO synthase (NOS) significantly reduces endothelium-dependent vasodilation in the renal bed, with an additional role of prostanoid revealed by inhibition of cyclooxygenase (COX) (30). Following inhibition of NOS and COX, there remains a vasodilator response to endothelial stimulation by A...

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Section: Discussionmentioning

confidence: 99%

In vivo regulation of endothelium-dependent vasodilation in the rat renal circulation and the effect of streptozotocin-induced diabetes

Edgley

Tare²,

Evans³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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“…The experiments described here were performed 9 months after the injection. Nine months after the administration of STZ (diabetic group) or buffer (control group), plasma glucose was determined using a commercially available enzyme kit (Wako Chemical Company, Osaka, Japan), as reported previously (Kobayashi et al, 2006;Matsumoto et al, 2006b).…”

Section: Animal Model Of Diabetesmentioning

confidence: 99%

Effect of long-term streptozotocin-induced diabetes on coronary vasoconstriction in isolated perfused rat heart

Kamata

Ozawa

Kobayashi

et al. 2008

J. Smooth Muscle Res.

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The primary goal of this study was to investigate the effect of long-term (9 months) streptozotocin (STZ)-induced diabetes on the coronary vasoconstrictor responses to vasoactive agents such as high K(+), acetylcholine (ACh), endothelin-1 (ET-1), and the calcium-channel activator Bay K 8644. For this, we used isolated rat hearts perfused at constant flow rate. Each of the four agents caused dose-dependent increases in perfusion pressure in isolated hearts from age-matched control and STZ-induced diabetic rats. The dose-response curves for high K(+), ACh, and ET-1 were shifted to the left, so that at some lower doses of these agents the increased perfusion pressure was greater in coronary arteries obtained from diabetic rats than in those from control rats. On the other hand, the maximum contractile response induced by each of these agents was lower in the diabetic perfused heart. The Bay K 8644-induced contractile response was significantly greater in the coronary arteries of diabetic rats than in those of control rats. A threshold-constrictor concentration of Bay K 8644 (1 nM) potentiated the ACh-induced vasoconstriction in coronary arteries from both groups, and the potentiated responses were greater in diabetic rats than in controls at lower concentrations of ACh (100 nM and 1 microM). These findings suggest that the coronary artery contractile responses to lower concentrations of ACh or ET-1 are exaggerated in long-term STZ-induced diabetic hearts. These changes may be due to alterations in the activity of voltage-gated Ca(2+) channels.

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“…Indeed, diabetes-induced impairment of endothelial function is a systemic phenomenon (23,29) observed in the brachial artery (30), the coronaries (31), as well as in vessels used as grafts in CABG, such as internal mammary arteries (23) and saphenous veins (32). Endothelial dysfunction in DM is multifactorial in nature, including decreased NO synthesis (33) and increased NO breakdown due to the higher oxidative stress status (34,35).…”

Section: Dm and Vasospasm In Rasmentioning

confidence: 99%

Diabetes Mellitus as a Predictor for Radial Artery Vasoreactivity in Patients Undergoing Coronary Artery Bypass Grafting

Choudhary

Antoniades

Brading

et al. 2007

Journal of the American College of Cardiology

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Changes in aortic endothelial gene expressions and relaxation responses following chronic short-term insulin treatment in diabetic rats

Cited by 14 publications

References 38 publications

In vivo regulation of endothelium-dependent vasodilation in the rat renal circulation and the effect of streptozotocin-induced diabetes

In vivo regulation of endothelium-dependent vasodilation in the rat renal circulation and the effect of streptozotocin-induced diabetes

Effect of long-term streptozotocin-induced diabetes on coronary vasoconstriction in isolated perfused rat heart

Diabetes Mellitus as a Predictor for Radial Artery Vasoreactivity in Patients Undergoing Coronary Artery Bypass Grafting

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